ライフサイエンスコーパス: DNA-damaging agent

1 s measured using the SOS-Chromotest (detects DNA-damaging agents).

2 erase beta that works synergistically with a DNA damaging agent.

3 mitochondria and nucleus in response to this DNA-damaging agent.

4 RP inhibitors alone or in combination with a DNA-damaging agent.

5 SW48) that were untreated or treated with a DNA-damaging agent.

6 iscovery to benefit cancer therapies using a DNA-damaging agent.

7 t effects of ionizing radiation, among other DNA damaging agents.

8 eases BER efficiency and sensitizes cells to DNA damaging agents.

9 in additive hypersensitivity to a variety of DNA damaging agents.

10 ion checkpoint response, upon treatment with DNA damaging agents.

11 t that TCOF1 promotes cellular resistance to DNA damaging agents.

12 ssing SSB-IDL fusions are sensitized to some DNA damaging agents.

13 ell morphology, and increased sensitivity to DNA damaging agents.

14 1 complex6 cause hypersensitivity to various DNA damaging agents.

15 ponses to targeted inhibitors of BRAF/MEK or DNA damaging agents.

16 rs and promotes cell survival in the face of DNA damaging agents.

17 e loci such as centromeres in the absence of DNA damaging agents.

18 ingly, POH1-deficient cells are sensitive to DNA damaging agents.

19 y apoptosis even in the absence of exogenous DNA damaging agents.

20 oprine may contribute as photosensitizing or DNA damaging agents.

21 both Gcn5 and Rtt109 are highly sensitive to DNA damaging agents.

22 e of active PARP1 in vitro or in response to DNA damaging agents.

23 n slow growth and renders cells sensitive to DNA damaging agents.

24 that are targeted by subsequent exposure to DNA damaging agents.

25 ons induced by both endogenous and exogenous DNA damaging agents.

26 renders cells highly sensitive to a range of DNA damaging agents.

27 with topoisomerase II poisons but not other DNA damaging agents.

28 2 function is associated with sensitivity to DNA damaging agents.

29 t in enhanced sensitivity to a wide range of DNA damaging agents.

30 ymes increases cancer cell susceptibility to DNA damaging agents.

31 are hypersensitive to genotoxicity caused by DNA damaging agents.

32 results in cell death or hypersensitivity to DNA damaging agents.

33 e2w alone are not hypersensitive to the same DNA damaging agents.

34 s causes either sensitivity or resistance to DNA-damaging agents.

35 are hypersensitive to genotoxicity caused by DNA-damaging agents.

36 se I-dependent manner, which is activated by DNA-damaging agents.

37 common type of environmental and endogenous DNA-damaging agents.

38 and growth advantage, following exposure to DNA-damaging agents.

39 and is under LexA control, being induced by DNA-damaging agents.

40 cient mice (SKO) are prone to CAC induced by DNA-damaging agents.

41 lar resistance of BRCA1 wild-type tumours to DNA-damaging agents.

42 ested the deletion strain for sensitivity to DNA-damaging agents.

43 ls can be exploited for cancer therapy using DNA-damaging agents.

44 d apoptosis in response to certain exogenous DNA-damaging agents.

45 downstream function of WEE1 upon exposure to DNA-damaging agents.

46 an cancers, confers resistance to killing by DNA-damaging agents.

47 omic instability and enhanced sensitivity to DNA-damaging agents.

48 during normal replication and in response to DNA-damaging agents.

49 me of patients with NPC who are treated with DNA-damaging agents.

50 4 proteins and resistance to cell killing by DNA-damaging agents.

51 se RNA, which is altered upon treatment with DNA-damaging agents.

52 OS levels and by exposing cells to oxidative DNA-damaging agents.

53 ortant for survival of cells challenged with DNA-damaging agents.

54 ponsible for the acquired resistance against DNA-damaging agents.

55 al to block DNA repair and therefore enhance DNA-damaging agents.

56 SP1 deubiquitinating enzyme upon exposure to DNA-damaging agents.

57 maintaining genomic integrity in response to DNA-damaging agents.

58 RNF4 gene displayed increased sensitivity to DNA-damaging agents.

59 repair genes and enhanced cell resistance to DNA-damaging agents.

60 uclear foci patterns observed in response to DNA-damaging agents.

61 d differentially to doxycycline, hypoxia, or DNA-damaging agents.

62 itro and (ii) treatment of cancer cells with DNA-damaging agents.

63 ransformation and survival after exposure to DNA-damaging agents.

64 ble to resensitize PRMT7 knock-down cells to DNA-damaging agents.

65 itor) that sensitizes p53-deficient cells to DNA-damaging agents.

66 romatin after DNA damage or to resistance to DNA-damaging agents.

67 E cells were exposed to mitomycin C or other DNA-damaging agents.

68 nd does not trigger apoptosis in response to DNA-damaging agents.

69 esponse and, thus, sensitize cancer cells to DNA-damaging agents.

70 ed breaks, and recN mutants are sensitive to DNA-damaging agents.

71 d increases the efficacy of chemotherapeutic DNA-damaging agents.

72 olaparib sensitized ATM null tumor cells to DNA-damaging agents.

73 ity syndrome characterized by sensitivity to DNA-damaging agents.

74 rexpression showed changes in sensitivity to DNA-damaging agents.

75 e p53-mediated growth inhibitory response to DNA-damaging agents.

76 in RNA and increases cellular sensitivity to DNA-damaging agents.

77 anner and greatly exacerbated sensitivity to DNA-damaging agents.

78 nes and found that the most potent drugs are DNA-damaging agents.

79 demonstrate an intrinsic supersensitivity to DNA-damaging agents.

80 ed for cell viability upon acute exposure to DNA-damaging agents.

81 upon DNA damage, RRP1B is induced by several DNA-damaging agents.

82 abolism and is phosphorylated in response to DNA-damaging agents.

83 expression of ALC1 results in sensitivity to DNA-damaging agents.

84 hase I trials of ABT-888 in combination with DNA-damaging agents.

85 ize tumors to the effects of taxanes but not DNA-damaging agents.

86 phase DSBs, and increased the sensitivity to DNA-damaging agents.

87 s apoptosis to both endogenous and exogenous DNA-damaging agents.

88 tigate their potential as radical-generating DNA-damaging agents.

89 to predict cellular resistance to killing by DNA-damaging agents.

90 genomic instability and drives resistance to DNA-damaging agents.

91 the genome and showed higher sensitivity to DNA-damaging agents.

92 oisomerase inhibitors and a variety of other DNA-damaging agents.

93 the pericentromere expands after exposure to DNA-damaging agents.

94 ant flies or their survival upon exposure to DNA-damaging agents.

95 SH2 from cells renders resistance to certain DNA-damaging agents.

96 ient cells display heightened sensitivity to DNA-damaging agents.

97 s proliferation and confers sensitization to DNA-damaging agents.

98 esulting in hypersensitivity to a variety of DNA damaging agents, a diminished ability to maintain re

99 Finally, we show that a variety of DNA damaging agents all result in a large increase in FB

100 , persistent RAD51 foci, hypersensitivity to DNA damaging agents and accumulation of DNA strand break

101 nance of genome integrity, for resistance to DNA damaging agents and for gene targeting.

102 alpha-helix and observed hypersensitivity to DNA damaging agents and increased frequency of genome re

103 nockdown in vitro sensitizes cancer cells to DNA damaging agents and induces cell death via p53-depen

104 an cells lacking HPF1 exhibit sensitivity to DNA damaging agents and PARP inhibition, thereby suggest

105 may be responsible for their sensitivity to DNA damaging agents and poly-(ADP)-ribose polymerase inh

106 ransformed cells are not more susceptible to DNA damaging agents and repair DNA lesions at a rate sim

107 yper-recombination phenotype, sensitivity to DNA damaging agents and synthetic lethality with mutatio

108 wn of CEP164 or ZNF423 causes sensitivity to DNA damaging agents and that cep164 knockdown in zebrafi

109 ants display sensitivity to a broad range of DNA-damaging agents and cell wall-targeting antibiotics.

110 This results in sensitivity to DNA-damaging agents and chromosomal instabilities.

111 ignificantly reduces cellular sensitivity to DNA-damaging agents and decreases cellular DNA mismatch

112 HARP results in hypersensitivity to multiple DNA-damaging agents and defects in fork stability or res

113 n addition, we have counter-screened several DNA-damaging agents and demonstrate that the Topo2a-depe

114 apoptosis by expression of IAP-antagonists, DNA-damaging agents and even knockdown of the IAP diap1.

115 roposed to sensitize hypoxic cancer cells to DNA-damaging agents and inhibitors of DNA repair.

116 se models to assess bone marrow toxicity for DNA-damaging agents and inhibitors of the DNA damage res

117 CCR5 reexpression augments resistance to DNA-damaging agents and is sufficient to induce cancer m

118 73A mutant conferred cellular sensitivity to DNA-damaging agents and led to defective repair of DNA d

119 p53 tumors utilizing a regimen consisting of DNA-damaging agents and mutp53 acetylators, which is cur

120 r rheostat that determines susceptibility to DNA-damaging agents and other death stimuli.

121 therapeutically exploited by treatment with DNA-damaging agents and PARP inhibitors.

122 air genes and subsequent hypersensitivity to DNA-damaging agents and PARP1/2 inhibitors.

123 apply to the entire family of monofunctional DNA-damaging agents and pave the way for rational improv

124 own to confer yeast cells with resistance to DNA-damaging agents and play a role in activation of DNA

125 devoid of Set2/H3K36me are hypersensitive to DNA-damaging agents and site-specific DSBs, fail to prop

126 eficient tumor cells to apoptosis induced by DNA-damaging agents and suggests that disruption of cryp

127 es established predicted hypersensitivity to DNA-damaging agents and were associated with mutations i

128 s and cell survival following treatment with DNA-damaging agents and, as such, may play roles in modu

129 mpaction was proportional to the dose of the DNA damaging agent, and results obtained in cells defect

130 ional silencing and increased sensitivity to DNA damaging agents, and these defects are exacerbated w

131 enzymes, DNA repair capacity, sensitivity to DNA-damaging agents, and iron homeostasis.

132 affects genomic instability, sensitivity to DNA-damaging agents, and migration of tumor cells by rec

133 ess, are more tolerant than the wild type to DNA-damaging agents, and show constitutive induction of

134 s but also recognizes DNA adducts induced by DNA-damaging agents, and triggers cell-cycle arrest and

135 Most DNA-damaging agents are weak inducers of an anticancer i

136 ion olaparib PARP inhibitor and temozolomide DNA-damaging agent as an effective therapy for rhabdomyo

137 and subcellular localization in response to DNA damaging agents at the single-cell level.

138 in the cytoplasm and, after treatment with a DNA-damaging agent, at the centrosomes.

139 -tailed SSB recovers faster from exposure to DNA damaging agents but accumulates more mutations.

140 Cells lacking CHIP are hypersensitive to DNA-damaging agents, but DNA repair and cell viability a

141 ficient cells, do not exhibit sensitivity to DNA-damaging agents, but do display shortened (but stabl

142 igG sigma factor was induced by a variety of DNA-damaging agents, but inactivation of sigG did not af

143 e apoptotic properties of a chemotherapeutic DNA-damaging agent by regulating the expression, subcell

144 ficient tumors in order to sensitize them to DNA-damaging agents by eliminating Chk1-mediated checkpo

145 of this complex confers hypersensitivity to DNA-damaging agents by undefined mechanisms.

146 in CML and non-CML cells upon treatment with DNA damaging agent camptothecin.

147 Noxa were required for apoptosis induced by DNA damaging agents camptothecin and UV.

148 l mouse cortical neurons, treatment with the DNA-damaging agent camptothecin (CPT) resulted in elonga

149 ockdown exacerbated apoptosis induced by the DNA-damaging agent camptothecin.

150 tc3 exhibit synergistic sensitivities to the DNA-damaging agents camptothecin and methyl methanesulfo

151 d that the conjugation of antiangiogenic and DNA-damaging agents can generate potential hybrid agents

152 DNA-damaging agents can induce premature senescence in c

153 roso compounds (NOCs), an important class of DNA damaging agents, can induce the carboxymethylation o

154 ation of gammaH2AX foci after treatment with DNA-damaging agents cannot, therefore, be used as a dire

155 iates resistance to apoptosis in response to DNA-damaging agents, causing BRCA1 wild-type tumours to

156 Upon exposure to DNA-damaging agents, cells expressing non-phosphorylatab

157 When fission yeast cells are treated with DNA-damaging agents, Chk1 is activated and phosphorylate

158 utations were somewhat less sensitive to the DNA-damaging agent ciprofloxacin than the corresponding

159 RNA)-rich nucleoli in cells treated with the DNA-damaging agents cisplatin and etoposide.

160 )histone2AX (gammaH2AX) after treatment with DNA damaging agents, compared with T cells from controls

161 p12, which occurs in cells upon exposure to DNA-damaging agents, converts Pol delta to a form that h

162 were used to investigate the effects of the DNA-damaging agent cumene-hydroperoxide (cum-OOH) and a

163 SETD2 mutations led to resistance to DNA-damaging agents, cytarabine, 6-thioguanine, doxorubi

164 eferred cancer regimens combine a MTA with a DNA-damaging agent (DDA).

165 DNA-damaging agents (DDAs) constitute the backbone of tr

166 linked to the resistance of cancer cells to DNA-damaging agents (DDAs).

167 THRAP3 and/or BCLAF1 leads to sensitivity to DNA damaging agents, defective DNA repair and genomic in

168 dogenous p53-target genes in response to the DNA damaging agent doxorubicin.

169 O(2)) in combination with the antineoplastic DNA-damaging agents doxorubicin, cisplatin, olaparib, an

170 d that AZD1775 alone and in combination with DNA-damaging agents (e.g., cisplatin and radiation) decr

171 We show that infection in the presence of DNA-damaging agents enhances infection and triple-negati

172 nt isogenic cell lines to a diverse panel of DNA-damaging agents, enriched for chemotherapeutics.

173 nes toward the induction of apoptosis by the DNA-damaging agent etoposide.

174 approximately 20%) following exposure to the DNA-damaging agent etoposide.

175 emonstrate that following treatment with the DNA-damaging agents, etoposide or camptothecin, BRCA1 is

176 ent of ARPE-19 diploid epithelial cells with DNA-damaging agents, etoposide or zeocin, induces HSATII

177 ree H3 and H4 concomitant with resistance to DNA damaging agents, even in mutants defective in the DN

178 The addition of a DNA-damaging agent further upregulated p53 protein level

179 DC1, NBS1, mTR or hMLH1) or cells exposed to DNA-damaging agents had elevated IGF-1 expression, resul

180 AZD1775 and DNA-damaging agents have displayed favorable activity in

181 stem cells showed sensitivity to a range of DNA-damaging agents, highlighting its role in replicatio

182 mES cells and their effect on sensitivity to DNA-damaging agents, homologous recombination and genomi

183 /BRCA2 loss of function mutations respond to DNA damaging agents, however, some do not.

184 hibition of mTOR results in sensitization to DNA-damaging agents; however, the molecular mechanism is

185 on when assessed for hypersensitivity to the DNA-damaging agent hydroxyurea (HU).

186 PARGi synergized with DNA-damaging agents (i.e., oxaliplatin and 5-fluorouraci

187 inistration of an ATR kinase inhibitor and a DNA damaging agent impacts the DNA damage induced by the

188 RG depletion causes sensitisation to certain DNA damaging agents, implicating PARG as a potential the

189 he four mammalian FoxO genes, in response to DNA damaging agents in both mouse embryonic fibroblasts

190 l biomarker to predict primary resistance to DNA damaging agents in patients with germline BRCA1 and

191 ese results suggest that Al likely acts as a DNA-damaging agent in vivo and that Al-dependent root gr

192 suggest that BRN2 may impact the response to DNA-damaging agents in BRN2-expressing cancers.

193 evere phenotypic effects with sensitivity to DNA-damaging agents in fission yeast and reduced viabili

194 mbination of allosteric PARP inhibitors with DNA-damaging agents in genomically unstable cancer cells

195 vide a clinical application for AZD1775 with DNA-damaging agents in KRAS/LKB1 NSCLC.

196 The causes of sensitivity to DNA-damaging agents in nondividing cell populations, suc

197 enes may be exploited to optimize the use of DNA-damaging agents in patients with high-risk MM.

198 HuR's role in the efficacy of DNA-damaging agents in PDA cells was, in part, attribute

199 gly potentiates the efficacy of a variety of DNA-damaging agents in preclinical models.

200 , PD-1 and CTLA-4 and greater sensitivity to DNA-damaging agents in representative cell line models;

201 that mESCs are fully viable and resistant to DNA-damaging agents in those conditions.

202 and sensitized p53-deficient cancer cells to DNA-damaging agents in vitro and in vivo.

203 n cells leads to an increased sensitivity to DNA-damaging agents, in particular interstrand cross-lin

204 nstrated that ERbeta sensitizes GBM cells to DNA damaging agents including temozolomide (TMZ).

205 Since we previously showed that DNA-damaging agents (including chemotherapy and irradiat

206 ta and bdf2Delta cells showed sensitivity to DNA damaging agents, including camptothecin, that cause

207 levels in E. coli cells exposed to exogenous DNA damaging agents, including many commonly used antibi

208 DNA and rendered parasites more sensitive to DNA-damaging agents, including ART.

209 ation and consequently are hypersensitive to DNA-damaging agents, including cisplatin and poly(ADP-ri

210 own preclinical activity in combination with DNA-damaging agents, including radiotherapy and topoisom

211 ane lesion (DOB) is produced by a variety of DNA-damaging agents, including the aforementioned.

212 ta60 supports normal growth and responses to DNA damaging agents, indicating that Smc5/6 does not sim

213 early S phase and are sensitive to multiple DNA-damaging agents, indicating impaired DNA replication

214 Here we show that bulky DNA damaging agents induce localized fork stalling at ye

215 Moreover, DNA-damaging agents induce ABH8 expression in an ATM-dep

216 olog 7 (ALKBH7) gene plays a pivotal role in DNA-damaging agent-induced programmed necrosis by trigge

217 of this variant transforms a bacteriostatic DNA damaging agent into a bactericidal drug, resulting i

218 An effective response to DNA damaging agents involves modulating numerous facets

219 hk1 could potentiate the cytotoxicity of the DNA damaging agent irinotecan in TNBC using xenotranspla

220 is and show that REV3-mediated resistance to DNA-damaging agents is independent of the replication da

221 enomic stability in the absence of exogenous DNA-damaging agents is unclear.

222 doxorubicin, and etoposide, but not to a non-DNA damaging agent, l-asparaginase.

223 ion, C646 is shown to promote sensitivity to DNA damaging agents, leading to the enhanced apoptosis o

224 pleted of NFKBIL2 or MMS22L are sensitive to DNA-damaging agents, load phosphorylated RPA onto chroma

225 sed by the sni1 mutation or treatment with a DNA-damaging agent markedly enhances SA-mediated defense

226 We focus on genomic responses to the DNA damaging agent methyl methanesulfonate (MMS) in comp

227 in recombination rates and resistance to the DNA damaging agent methyl methanesulfonate, suggesting t

228 h54 is not necessary for the response to the DNA-damaging agent methyl methanesulfonate.

229 e DNA replication stress than by the general DNA-damaging agent methyl methanesulfonate.

230 opper genes are regulated in response to the DNA-damaging agents methyl methanesulfonate (MMS) and hy

231 aradoxically, analysis of cells resistant to DNA damaging agents missing the CTD restore HR proficien

232 ) results in an increased sensitivity to the DNA damaging agent mitomycin C (MMC) that correlates wit

233 mrfA and mrfB results in sensitivity to the DNA damaging agent mitomycin C, but not to any other typ

234 lease activity, and affects tolerance to the DNA-damaging agent mitomycin C, argue that this prototyp

235 reduced their viability upon exposure to the DNA-damaging agents mitomycin C and Irofulven, but not e

236 cacy of MK-1775 alone or in combination with DNA damaging agents (MMC or oxaliplatin) in PDA cell lin

237 shown to be sensitive to treatment with the DNA damaging agent MMS.

238 Upon addition of a DNA-damaging agent, MMSET-high cells repaired DNA damage

239 a protects against cell death induced by the DNA damaging agent N-methyl-N-nitro-N-nitrosoguanidine (

240 utation are sensitive to radiation and other DNA-damaging agents, no such individual has yet develope

241 Upon exposure of human cells to DNA-damaging agents, NUCKS1 controls the resolution of R

242 types of transformed cells exposed to either DNA damaging agents or CDK4 inhibitors.

243 f cohesin become SUMOylated upon exposure to DNA damaging agents or presence of a DNA double-strand b

244 Exposure of neurons to DNA damaging agents or the excitotoxin NMDA elicited sim

245 athways through transcriptional responses to DNA damaging agents or through predicted miRNA regulatio

246 1 was generated by treatment of cells with a DNA-damaging agent or by addition of NAD(+) to CFEs.

247 R genes, providing a rationale for combining DNA-damaging agents or targeted DDR inhibitors with horm

248 lustering of damage is a hallmark of certain DNA-damaging agents, particularly ionizing radiation.

249 tumorigenicity and tumor cell resistance to DNA damaging agents, properties associated with tumor-in

250 Exposure of cells to DNA-damaging agents results in a rapid increase in the f

251 rigin firing is blocked by prior exposure to DNA damaging agents showing that the prevention of origi

252 Characterization of the direct effects of DNA-damaging agents shows how DNA lesions lead to specif

253 Loss of RecO elicits hypersensitivity to DNA damaging agents similar to that caused by deletion o

254 e, CHK1i sensitizes CHK1i-resistant cells to DNA damaging agents such as gemcitabine or hydroxyurea b

255 strated to enhance the anti-tumor effects of DNA damaging agents such as gemcitabine.

256 DNA repair and enhances the genotoxicity of DNA-damaging agents such as benzo[a]pyrene and ultraviol

257 n turn, cellular response to treatments with DNA-damaging agents such as cisplatin (cis-dichlorodiamm

258 in turn, cellular response to treatment with DNA-damaging agents such as cisplatin, ionizing radiatio

259 us, BRCA-associated cancers are sensitive to DNA-damaging agents such as cisplatin.

260 en Escherichia coli grows in the presence of DNA-damaging agents such as methyl methanesulphonate (MM

261 ination (HR) DNA repair and are sensitive to DNA-damaging agents such as platinum and PARP inhibitors

262 remains unchanged after cells are exposed to DNA-damaging agents such as UV light (generating UV phot

263 n was distinct from that of more traditional DNA damaging agents, such as camptothecin, as it was p53

264 hibitors also prevent recovery from multiple DNA-damaging agents, suggesting broad applicability for

265 In contrast, the DNA damaging agent temozolomide (TMZ), which is used as

266 ponse to treatment with the chemotherapeutic DNA-damaging agent temozolomide.

267 eptible to apoptosis induced by etoposide, a DNA-damaging agent, than HIPK2+/+ cells.

268 ignancies by promoting cellular responses to DNA damaging agents that are currently ineffective again

269 his mechanism provides the impetus to design DNA damaging agents that produce DSBs by abstracting a s

270 a chemical basis for the cytotoxicity of the DNA damaging agents that produce this lesion.

271 A DNA-damaging agent that induces DNA double-stranded brea

272 mines formed in well-done cooked meats, as a DNA-damaging agent that may contribute to the etiology o

273 y with a single-strand break by a variety of DNA-damaging agents that abstract a hydrogen atom from t

274 and Rad3-related (ATR) gene is activated by DNA-damaging agents that are frequently used as anticanc

275 interactions between kinase deficiencies and DNA-damaging agents that are used as chemotherapeutics.

276 2 in B. subtilis sensitized cells to several DNA-damaging agents that can block or impair replication

277 ARCAL1-depleted cells display sensitivity to DNA-damaging agents that induce replication fork collaps

278 Lig3-null cells are not sensitive to several DNA-damaging agents that sensitize Xrcc1-deficient cells

279 ssion is required for the normal response to DNA-damaging agents, the nuclear localisation of RAD51 a

280 tins) are unsaturated imines that are potent DNA damaging agents, thereby confirming an earlier mecha

281 ils) are required for cellular resistance to DNA damaging agents; therefore, we examined the role of

282 recipitated senescence following exposure to DNA-damaging agents, thus accounting for higher sensitiv

283 ective WEE1 inhibitor MK-1775 synergize with DNA-damaging agent to inhibit cancer cell growth.

284 b at the BRCA1 promoter that is disrupted by DNA-damaging agents to increase its transcription.

285 kinase that is activated by a wide range of DNA-damaging agents to slow the cell cycle during S phas

286 1 foci formation, sensitizes cancer cells to DNA damaging agents, to Poly (ADP-ribose) polymerase (PA

287 3 that is sufficient, even in the absence of DNA-damaging agents, to increase the expression of proap

288 ) in cellular responses to chronic, low-dose DNA-damaging agent treatment by maintaining MEFs in low

289 However, combined Nutlin3a and chronic DNA-damaging agent treatment is insufficient to promote

290 owever, it is still unclear how CSCs survive DNA-damaging agent treatment.

291 machinery and, consequently, the response to DNA-damaging agents used routinely in the clinic.

292 Histone deacetylase (HDAC) inhibitors and DNA-damaging agents were identified as novel Golgi disru

293 r hypersensitivity to replication stress and DNA-damaging agents when combined with mutations in hist

294 non-homologous end joining, and tolerance to DNA-damaging agents when other resection enzymes are abs

295 ent on CDK4/6 were resistant to IR and other DNA-damaging agents when treated with CDK4/6 inhibitors.

296 tion and exposure of cells to mitomycin C, a DNA damaging agent, which interferes with FtsZ ring asse

297 ncreased level of DNA-PKcs and resistance to DNA damaging agents, which is reversed by a DNA-PK inhib

298 wn to provide resistance to a broad range of DNA-damaging agents while also contributing to mismatch

299 be used to measure variations in response to DNA damaging agents within the same cell population.

300 ge response and to sensitize cancer cells to DNA-damaging agents without affecting other functions of